scholarly journals Plant and animal PR1 family members inhibit programmed cell death and suppress bacterial pathogens in plant tissues

2018 ◽  
Vol 19 (9) ◽  
pp. 2111-2123 ◽  
Author(s):  
James E. Lincoln ◽  
Juan P. Sanchez ◽  
Kristina Zumstein ◽  
David G. Gilchrist
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Bacterial Pathogens ◽  
Family Members ◽  
Plant Tissues

Differential regulation of transcription and induction of programmed cell death by human p53-family members p63 and p73

FEBS Letters ◽  
2002 ◽  
Vol 525 (1-3) ◽  
pp. 93-99 ◽  
Author(s):  
Sebastian Dietz ◽  
Karen Rother ◽  
Casimir Bamberger ◽  
Hartwig Schmale ◽  
Joachim Mössner ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Differential Regulation ◽  
Regulation Of Transcription ◽  
P53 Family

BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death

2002 ◽  
Vol 115 (8) ◽  
pp. 1567-1574 ◽  
Author(s):  
Philippe Bouillet ◽  
Andreas Strasser
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Protein Family ◽  
Cell Stress ◽  
Protective Function ◽  
Evolutionarily Conserved ◽  
Apoptotic Cascade

The BH3-only members of the Bcl-2 protein family are essential initiators of programmed cell death and are required for apoptosis induced by cytotoxic stimuli. These proteins have evolved to recognise distinct forms of cell stress. In response, they unleash the apoptotic cascade by inactivating the protective function of the pro-survival members of the Bcl-2 family and by activating the Bax/Bax-like pro-apoptotic family members.

Promoter cloning and characterization of the human programmed cell death protein 4 (pdcd4) gene: evidence for ZBP-89 and Sp-binding motifs as essential Pdcd4 regulators

2012 ◽  
Vol 32 (3) ◽  
pp. 281-297 ◽  
Author(s):  
Jörg Hendrik Leupold ◽  
Irfan Ahmed Asangani ◽  
Giridhar Mudduluru ◽  
Heike Allgayer
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Promoter Activity ◽  
Family Members ◽  
Tumour Suppressor ◽  
Solid Cancer ◽  
Basal Region ◽  
Mobility Shift ◽  
Basal Promoter Activity ◽  
Cell Death Protein

Pdcd4 (programmed cell death protein 4) is an important novel tumour suppressor inhibiting transformation, translation, invasion and intravasation, and its expression is down-regulated in several cancers. However, little is known about the transcriptional regulation and the promoter of this important tumour suppressor. So far the following is the first comprehensive study to describe the regulation of Pdcd4 transcription by ZBP-89 (zinc-finger-binding protein 89), besides characterizing the gene promoter. We identified the transcriptional start sites of the human pdcd4 promoter, a functional CCAAT-box, and the basal promoter region. Within this basal region, computer-based analysis revealed several potential binding sites for ZBPs, especially for Sp (specificity protein) family members and ZBP-89. We identified four Sp1/Sp3/Sp4-binding elements to be indispensable for basal promoter activity. However, overexpression of Sp1 and Sp3 was not sufficient to enhance Pdcd4 protein expression. Analysis in different solid cancer cell lines showed a significant correlation between pdcd4 and zbp-89 mRNA amounts. In contrast with Sp transcription factors, overexpression of ZBP-89 led to an enhanced expression of Pdcd4 mRNA and protein. Additionally, specific knockdown of ZBP-89 resulted in a decreased pdcd4 gene expression. Reporter gene analysis showed a significant up-regulation of basal promoter activity by co-transfection with ZBP-89, which could be abolished by mithramycin treatment. Predicted binding of ZBP-89 to the basal promoter was confirmed by EMSA (electrophoretic mobility-shift assay) data and supershift analysis for ZBP-89. Taken together, data for the first time implicate ZBP-89 as a regulator of Pdcd4 by binding to the basal promoter either alone or by interacting with Sp family members.

ROLE OF BH3-ONLY PRO-APOPTOTIC BCL-2 FAMILY MEMBERS IN PROGRAMMED CELL DEATH AND PATHOLOGY

Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 53
Author(s):  
A Strasser ◽  
P. Bouillet ◽  
A. Villunger ◽  
L Coultas ◽  
E Michalak
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members

scholarly journals Dealing with the problem of non-specific in situ mRNA hybridization signals associated with plant tissues undergoing programmed cell death

Plant Methods ◽  
2010 ◽  
Vol 6 (1) ◽  
pp. 7 ◽  
Author(s):  
Jaana Vuosku ◽  
Suvi Sutela ◽  
Mira Sääskilahti ◽  
Johanna Kestilä ◽  
Anne Jokela ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Plant Tissues ◽  
Mrna Hybridization ◽  
In Situ Mrna Hybridization

scholarly journals Apoptosis in Hydra: function of HyBcl-2 like 4 and proteins of the transmembrane BAX inhibitor motif (TMBIM) containing family

2019 ◽  
Vol 63 (6-7) ◽  
pp. 259-270 ◽  
Author(s):  
Mina Motamedi ◽  
Laura Lindenthal ◽  
Anita Wagner ◽  
Margherita Kemper ◽  
Jasmin Moneer ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Epithelial Cells ◽  
Programmed Cell Death ◽  
Kinase Inhibitor ◽  
Apoptotic Cell ◽  
Family Members ◽  
Sequence Comparisons ◽  
Induced Apoptosis ◽  
Related Proteins

Mechanisms of programmed cell death differ between animals, plants and fungi. In animals, apoptotic cell death depends on caspases and Bcl-2 family proteins. These protein families are only found in multicellular animals, including cnidarians, insects and mammals. In contrast, members of the TMBIM-family of transmembrane proteins are conserved across all eukaryotes. Sequence comparisons of cell death related proteins between phyla indicate strong conservation of the genes involved. However, often it is not known whether this is paralleled by conservation of function. Here we present the first study to support an anti-apoptotic function of Bcl-2 like proteins in the cnidarian Hydra within a physiological context. We used transgenic Hydra expressing GFP-tagged HyBcl-2-like 4 protein in epithelial cells. The protein was localised to mitochondria and able to protect Hydra epithelial cells from apoptosis induced by either the PI(3) kinase inhibitor wortmannin or by starvation. Moreover, we identified members of the TMBIM-family in Hydra including HyBax-Inhibitor-1, HyLifeguard-1a and -1b and HyLifeguard 4. Expressing these TMBIM-family members in Hydra and human HEK cells, we found HyBax-inhibitor-1 protein localised to ER-membranes and HyLifeguard-family members localised to the plasma membrane and Golgi-vesicles. Moreover, HyBax-inhibitor-1 protected human cells from camptothecin induced apoptosis. This work illustrates that the investigated Bcl-2- and TMBIM-family members represent evolutionarily conserved mitochondrial, ER, Golgi and plasma membrane proteins with anti-apoptotic functions. The participation of ER and Golgi proteins in the regulation of programmed cell death might be a very ancient feature.

scholarly journals Deficiency of Pro-apoptotic Hrk Attenuates Programmed Cell Death in the Developing Murine Nervous System but Does Not Affect Bcl-x Deficiency-Induced Neuron Apoptosis

2011 ◽  
Vol 59 (11) ◽  
pp. 976-983 ◽  
Author(s):  
Arindam P. Ghosh ◽  
Jennifer D. Cape ◽  
Barbara J. Klocke ◽  
Kevin A. Roth
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
System Development ◽  
Critical Role ◽  
Family Members ◽  
Nervous System Development ◽  
Neuronal Populations ◽  
Embryonic Nervous System ◽  
Induced Neuron

The BCL-2 family includes both pro- and anti-apoptotic proteins, which regulate programmed cell death during development and in response to various apoptotic stimuli. The BH3-only subgroup of pro-apoptotic BCL-2 family members is critical for the induction of apoptotic signaling, by binding to and neutralizing anti-apoptotic BCL-2 family members. During embryonic development, the anti-apoptotic protein BCL-XL plays a critical role in the survival of neuronal populations by regulating the multi-BH domain protein BAX. In this study, the authors investigated the role of Harakiri (HRK), a relatively recently characterized BH3-only molecule in disrupting the BAX-BCL-XL interaction during nervous system development. Results indicate that HRK deficiency significantly reduces programmed cell death in the nervous system. However, HRK deficiency does not significantly attenuate the widespread apoptosis seen in the Bcl-x−/− embryonic nervous system, indicating that other BH3-only molecules, alone or in combination, may regulate BAX activation in immature neurons.

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